Medical-surgical Nursing 1

Medical-Surgical Nursing

Fluids and Electrolytes Fluids 60% of an adult’s body weight is water Factors affecting body fluid composition: 1. Age 2. Gender 3. Body fat Fluid Compartments in the body: 1. Intracellular space -fluid in the cells -approximately 2/3 of the total body water -primarily located in the skeletal muscle mass 

2. Extracellular Space -body fluid outside the cells -divided into: a. intravascular >contains plasma >approximately 3L out of 6L blood volume b. interstitial >fluid that surrounds the cells >approximately 11-12L in an average adult c. transcellular >smallest division of the ECF >approximately 1L of fluid >CSF, synovial, pericardial, pleural, intraocular

Electrolytes 2 types: 1. Cations -sodium, potassium, calcium, magnesium and hydrogen ions 2. Anions -phosphate, bicarbonate, chloride  3 Pressures Important in the Maintenance of Fluid Balance 1. hydrostatic pressure 2. osmotic pressure 3. oncotic pressure 





Regulation of Body Fluid Compartments 1. Osmosis and Osmolality 2. Diffusion 3. Filtration 4. Sodium-Potassium Pump Routes of Gains and Losses 1. Kidneys >approximately 1L in an average adult >1mg/kg/hour 2. Skin >may vary from 0 – 1000ml or more 3. Lungs >approximately at 400ml a day

4. GI tract >at 100 – 200ml a day Laboratory Tests for Evaluating Fluid Status 1. Osmolality serum Na x 2= glu/18 +BUN/3= Approx value of serum osmolality Osmolarity 2. BUN 10 – 20mg/dl or 3.5 – 7 mmol/L 3. Creatinine 0.7 – 1.5 mg/dl or 60 – 130mmol/L 4. Hematocrit males: 0.44 - 0.52 females: 0.39 - 0.47 5. Urine Sodium 50 – 220mEq/24 hours

Homeostatic Mechanisms 1. Kidneys -filters 170L of blood a day -excretes only 1.5L of urine/24 hours 2. Heart and Blood Vessel Functions 3. Lungs 4. Pituitary Function 5. Adrenal Functions 6. Parathyroid Functions 7. Baroreceptors a. high pressure baroreceptors -in the aortic arc and carotid sinus -in the juxtaglomerular cells of the nephron

b. low pressure baroreceptors -in the cardiac atria (left atrium) 8. Renin - Angiotensin - Aldosterone System Liver > Angiotensinogen > Angiotensin (kidneys) renin Angiotensin 2 (lungs) > Aldosterone (adrenals) ACE 9. ADH and Thirst 10. Osmoreceptors 11. Atrial Natriuretic Peptide -at 20 – 77pg/ml (20 -77ng/L)

 

Third Space Fluid Shift Fluid Volume Deficit Dehydration >causes: a. inadequate intake b. abnormal fluid losses c. other causes -diabetes insipidus -osmotic diuresis -hemorrhage -coma >signs and symptoms: weight loss, poor skin turgor, oliguria, concentrated urine, postural hypotension

rapid heart rate, decreased CVP, cool clammy skin, inc temperature >assessment: BUN and Crea Hematocrit Serum elecrolytes Urine specific gravity Fluid Challenge Test >management: a. oral route of fluid replacement -preferred method b. IV route -isotonic then hypotonic



c. monitoring -weight, intake and output, V/S, CVP level of consciousness, breath sounds and skin color >nursing management: a. prevent fluid volume deficit b. correct fluid volume deficit Fluid Volume Excess -isotonic expansion of body water >cause: a. abnormal retention of water and sodium >s/sx: a. edema b. distended neck veins

c. crackles g. increased CVP d. tachycardia h. increased weight e. increased BP i. increased urine output f. increased PP j. shortness of breath >assessment: BUN CXR Hematocrit Serum Osmolality Serum Electrolytes >management: a. withholding excessive administration of IVF b. diuretics c. restriction of oral fluids (sodium)



1. Pharmacologic Therapy 2. Hemodialysis 3. Nutritional Therapy >nursing management: a. preventing fluid volume excess b. detecting and controlling fluid volume excess c. teaching patients about edema Sodium Deficit -refers to serum sodium level below 135mEq/L >causes: a. vomiting d. fistulas b. diarrhea e. sweating c. diuretics f. dilutional hyponatremia

>s/sx: similar to dehydration >assessment: serum sodium of less than 135mEq/L urine sodium SIADH - >20mEq/L sodium loss - <20mEq/L >management: a. sodium replacement -by mouth, NGT or through parenteral route -parenterally, must not exceed 12mEq/L in 24 hours > osmotic demyelination

b. SIADH -give Demeclocycline or Lithium c. water restriction -safer than sodium replacement



Sodium Excess -sodium level higher than 145mEq/L -can occur in patients with normal fluid volume or in those with FVE or FVD >causes: a. gain of sodium in excess of water (administration of hypertonic saline) b. loss of water in excess of sodium (unconscious, cognitively impaired individuals, diarrhea,hyperventilation, burns, diabetes insipidus, heat stroke and sea water drowning) >signs and symptoms: predominantly neurologic (cellullar dehydration)

Management: >serum sodium should be reduced at a rate of 0.51mEq/L 1. IVF Therapy -hypotonic solution or isotonic non saline solution 2. Diuretics 3. Desmopressin Acetate Nursing Management: 1. Look for the hidden sources of sodium 2. Monitor for: body temperature, thirst and level of consciousness 3. Prevent hypernatremia 4. Correct hypernatremia

Potassium Deficit -potassium serum level <3.5mEq/L causes: >alkalosis, GI losses, hyperaldosteronism, potassium losing diuretics, other drugs (corticosteroids, amphotericin B, carbenicillin and sodium penicillin), insulin hypersecretion, inability or unwillingness to eat a normal diet, magnesium depletion, Cushing’s syndrome signs and symptoms: >fatigue, anorexia, nausea, vomiting, muscle weakness, leg cramps, decreased bowel motility, paresthesias, dysrhythmias and increased sensitivity to digitalis, glucose intolerance 

Confirmatory tests: 1. Decreased serum potassium 2. ECG changes -flat or inverted T waves and depression of the ST segments -elevation of the U waves 3. Metabolic Alkalosis 4. Urine potassium concentration of >20mEq/24 hours Medical Management: 1. Potassium replacement therapy -if without abnormal potassium loss, 40-80mEqs/day -oral (Kalium Durule) or IV (K chloride, K phosphate or K acetate)

Nursing Management: 1. Monitoring for s/sx or progression of hypokalemia 2. Preventing hypokalemia 3. Correcting hypokalemia 4. Administering IV potassium -after adequate urine flow -20mEqs/hour or less -30-40mEqs/L and below unless severe



Potassium Excess -less common but more severe than hypokalemia -causes: >renal failure, excessive intake of potassium, infection, hyporaldosteronism and Addison’s disease, medications (KCl, heparin, ACE inhibitors, NSAIDS and K sparing diuretics) and acidosis -clinical manifestations: >dysrhythmias, skeletal muscle weakness and paralysis >CNS and PNS involvement >Flaccid quadriplegia, respiratory and speech muscle paralysis

Confirmatory tests: 1. ECG -peaked, narrow T waves, ST segment depression and a shortened QT interval -prolonged PR interval then absence of P wave 2. ABG 3. Serum potassium level increase Medical Management: 1. Monitoring of serum potassium with ECG findings 2. Emergency pharmacologic therapy >calcium gluconate or calcium chloride >sodium bicarbonate >insulin and glucose >beta 2 agonist 3. Dialysis

Nursing Management: 1. Monitoring 2. Preventing hyperkalemia 3. Correcting hyperkalemia Pseudohyperkalemia >use of tourniquet in an exercising muscle >marked leukocytosis and thrombocytosis >familial pseudohyperkalemia



Calcium Deficit -less than 8.5mg/dl of calcium in the serum -causes: >hypoparathyroidism >those who received citrated blood >pancreatitis, renal failure >vitamin D deficiency, magnesium deficiency >medullary thyroid carcinoma >low albumin levels, alkalosis and alcohol abuse -signs and symptoms: >tetany, seizures and mental changes -confirmatory test: >ECG- prolonged QT interval

Management: 1. Administer calcium salts -calcium carbonate, calcium chloride, calcium gluceptate Risks: a. Sloughing of tissues b. Bradycardia then cardiac arrest c. Digitalis toxicity 2. IVF but not normal saline or solutions containing phosphates and bicarbonate 3. Vitamin D therapy 4. Aluminum hydroxide, calcium acetate, calcium carbonate 5. Nutritional therapy 6. Screen for and treat hypomagnesemia

Nursing Management: 1. Monitor hypocalcemia for patients at risk 2. Airway management 3. Seizure precaution 4. Patient education -caffeine and alcohol decreases absorption -nicotine increases excretion -medications to decrease bone loss (alendronate, raloxifene and calcitonin)

Calcium Excess -with high mortality rate -causes: >malignancies and hyperparathyroidism >immobilization >use of Thiazide diuretics >milk-alkali syndrome >Vitamin A and D intoxication -signs and symptoms: *proportional to the elevation of serum calcium >muscle weakness, incoordination, anorexia and constipation >cardiac arrest

>dehydration >abdominal and/or bone pain >abdominal distention and paralytic ileus >excessive urination then polyuria >s/sx of PUD >changes in the LOC and mental status *hypercalcemic crisis Laboratory tests: 1. Serum calcium determination 2. ECG - shortening of the QT interval and ST segment - prolongation of the PR interval - dysrhythmias 3. Double antibody PTH test

4. X-Ray - osteoporosis 5. Sulkowitch test Management: 1. Pharmacologic therapy -dilute the serum calcium and promote its exc. (normal saline, administer phosphates, diuretics, calcitonin) -Cancer treatment -Corticosteroid therapy > to decrease bone turnover and tubular reabsorption -Biphosphonates (pamidronate) >causes myalgia, pyrexia and decreased WBC -Mithramycin >causes thrombocytopenia and nephrotoxicity and hepatotoxicity

-IV phosphates should be used with caution >Phospho-Soda, Neutra-Phos Nursing Management: 1. Monitor the s/sx 2. Increase mobility 3. Increase oral fluid intake

Chloride Deficit -serum chloride level below 96mEq/L -causes: >chloride deficient formulas, salt restricted diets >GI tube drainage, severe vomiting and diarrhea -signs and symptoms: >hypokalemia, hyponatremia and metabolic alkalosis (hyperexcitability of muscles, tetany, hyperactivity of deep tendon reflexes, weakness, twitching, muscle cramps, cardiac dysrhythmias, seizures and coma) -lab tests: >serum chloride determination

>serum potassium and sodium determination >ABG >urine chloride level decrease (normal value110-250mEq/L) -medical management: >chloride replacement normal saline and half strength saline >reevaluate the use of diuretics >nutritional therapy tomato juice, salty broth, canned vegetables, processed meats and fruits >restriction of free water intake >ammonium chloride

-nursing management >monitoring of intake and output, ABG determination values, serum electrolyte levels, LOC, muscle strength and movement >vital signs and respiratory assessments >patient education as regards to replacement therapy

Chloride Excess -serum chloride level higher than 106mEq/L -associated with hypernatremia, bicarbonate loss and metabolic acidosis -causes: >loss of bicarbonate (GI and/or renal) -signs and symptoms: >metabolic acidosis, hypervolemia and hypernatremia (tachypnea, weakness, lethargy, deep rapid respirations, diminished cognitive ability and hypertension) >decrease in CO, dysrhythmias and coma -lab tests: >serum sodium and chloride determination >ABG- Bicarbonate less than 22mEq/L

-normal anion gap (8-12mEq/L) >urine chloride concentration greater than 250mEq/L -medical management: >IVF therapy -Lactated Ringer’s Solution >IV sodium bicarbonate >Diuretics >Fluids, sodium and chloride restriction -nursing management: >monitoring V/S, ABG, I&O >assessment of neurologic, respiratory and cardiac functions >patient education as regards to nutrition

Acid-Base Balance

Normal blood pH -7.35 to 7.45  Blood pH compatible with life -6.80 to 7.80  Buffer Systems -maintains the blood pH by removing or releasing H+ ions 1. Bicarbonate-Carbonic Acid Buffer System -the major extracellular buffer system -Bicarbonate to Carbonic Acid Ratio is 20:1 2. Phosphate Buffer System 3. Plasma proteins, RBC and Hemoglobin 

Organs involved in HCO3-H2CO3 System: 1. Kidneys -activation is slower (hours to days) but more efficient -has the ability to regenerate and reabsorb or excrete bicarbonates -has the ability to retain or excrete H+ -in acidosis: excrete H+ and conserve bicarbonate -in alkalosis: retain H+ and excrete bicarbonate -cannot compensate in renal failure 2. Lungs -adjust ventilation in response to CO2 content of the blood -activation is faster but less efficient

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit) -low pH; low plasma bicarbonate -causes: >gain of hydrogen ions or loss of bicarbonate -2 forms: A. High Anion Gap Acidosis -due to the accumulation of the unmeasured anions (phosphates, sulfates and proteins) B. Normal Anion Gap Acidosis (hyperchloremic acidosis) -due to the direct loss of bicarbonates >diarrhea >diuretics >lower intestinal fistulas >renal ins.

>excessive administration of chloride >excessive administration of parenteral solution without bicarbonate -signs and symptoms: >headache, confusion, drowsiness >increased respiratory rate and depth >nausea and vomiting >peripheral vasodilatation and decreased CO >decreased BP, cold and clammy skin, dysrhythmias and shock -lab tests: >ABG - low bicarbonate level and a low pH >Serum potassium determination

>Anion Gap Calculation >ECG -medical management: >Eliminate excessive sources of chloride >Sodium bicarbonate -if pH is less than 7.1 -if bicarbonate is less than 10mEq/L >Serum potassium monitoring and reversal of potential hypokalemia >Reversal of potential hypocalcemia >Sodium Bicarbonate >Dialysis

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess) -high pH; high plasma bicarbonate concentration -causes: (due to gain of bicarbonates or loss of hydrogen ions) >vomiting or gastric suction- most common >diuretics- loop and thiazides >hyperaldosteronism and Cushing’s syndrome >excessive alkali ingestion or administration >villous adenoma and cystic fibrosis -signs and symptoms: >decreased calcium ionization (tingling of the fingers, toes, dizziness

and hypertonic muscles) >depressed respirations >atrial arrhythmias then ventricular arrhythmias >decreased motility then paralytic ileus -lab tests: >ABG - pH greater than 7.45 - bicarbonate greater than 26mEq/L >Serum potassium determination >Urinary chloride levels -medical management: >Chloride replacement (KCl) >IVF containing sufficient sodium and chloride >H2R antagonists- in GI suctioning

>Carbonic Anhydrase Inhibitors >I&O monitoring Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) -pH is less than 7.35; paCO2 is higher than 42mmHg -causes: (due to inadequate excretion of CO2 > elevated plasma CO2 > elevated plasma H2CO3) >acute pulmonary edema >sedative overdose >aspiration of foreign body >severe pneumonia >atelectasis >RDS >pneumothorax >MG, GBS

-signs and symptoms: >increased HR, RR, BP, mental cloudiness and feeling of fullness in the head >ventricular fibrillation >increased intracranial pressure, papilledema, dilated conjunctival blood vessels >hyperkalemia -lab tests: >ABG >Serum electrolyte determination >Chest X-Ray >ECG >Drug screen for overdose

-medical management: >Pharmacologic *bronchodilators *thrombolytics *antibiotics *anticoagulants >Pulmonary hygiene >Adequate hydration >Supplemental O2 with caution >Mechanical ventilation

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit) -arterial pH of greater than 7.45; PaCO2 of less than 38mmHg -causes: (due to hyperventilation > blowing off of CO2 > decreased plasma carbonic acid concentration) >extreme anxiety, hypoxemia, early phase of Aspirin intoxication, gram negative bacteremia and inappropriate ventilator settings >chronic hepatic insufficiency, cerebral tumors -signs and symptoms: >lightheadedness, inability to concentrate

>numbness and tingling from reduced ionized calcium >tinnitus, loss of consciousness >tachycardia, atrial and ventricular arrhythmias -lab tests: >ABG >Serum electrolyte determination -management: >breath slowly or into a closed system >sedatives

Acid – Base Disturbances and Compensation Disorder

Initial Event

Compensation

Respiratory Acidosis

↑PaCO2;↑or N HCO3;↓ pH

Kidneys eliminate H+ & retain HCO3

Respiratory Alkalosis

↓PaCO2;↓or N HCO3;↑pH

Kidneys conserve H+ & excrete HCO3

Metabolic Acidosis

↓or N PaCO2; ↓HCO3;↓ pH

Metabolic Alkalosis

↑or N PaCO2; ↑HCO3;↑ pH

↓Lungs eliminate CO2 & conserve HCO3 Lungs ↓to↑ PaCO2, kidneys conserve H+

Burns Autograft Heterograft Homograft Carboxyhemoglobin

Escharotomy Fasciotomy Rule of Nines

4 Major Goals Relating to Burns 1. Prevention 2. Institution of lifesaving measures for the severely burned person. 3. Prevention of disability and disfigurement through early, specialized, individual treatment.

4. Rehabilitation through reconstructive surgery and rehabilitation programs. Burn Categories Burns are sustained through 1. Thermal 1. Conduction 2. Chemical 2. Electromagnetic radiation 3. Radiation Skin destruction can lead to; 1. Increased fluid loss 2. Infection 3. Hypothermia

4. Scarring, change in body image 5. Compromised immunity 6. Changes in function

Classification of burns: A. According to burn depth: 1. Superficial Partial Thickness (Similar to First Degree Burn)

-causes: *sunburn *low intensity flash -involves the epidermis and possibly a portion of the dermis -signs and symptoms: *tingling *pain that is soothed by *hyperesthesia cooling *reddened *possibly blisters *minimal or no edema -complete recovery within a week; no scarring -peel off

2. Deep Partial thickness (Similar to Second Degree Burn) -causes: *scalds *flash flame -involves the epidermis, upper dermis, portion of the deeper dermis -s/sx: *pain *sensitive to cold air *hyperesthesia *blistered, weeping surface *broken epidermis *edema -recovery in 2-4 weeks -some scarring and depigmentation contractures -infection may convert it to full thickness

3. Full Thickness (Similar to Third Degree) -causes: *flame *prolonged exposure to hot liquids *electric current *chemical -involves the epidermis, entire dermis and sometimes subcutaneous tissue, may involve connective tissue, muscle and bone -s/sx: *pain free *hemolysis *shock *entrance and exit wounds *hematuria *broken skin with exposed *edema fats

-eschar sloughs -grafting necessary -scarring and loss of contour and function; contractures -loss of digits or extremity possible Physiologic Responses to Burns Local Pathophysiologic Response -if only less than 25% of the TBSA is involved Local and Systemic Pathophysiologic Response -if more than 25% of the TBSA is involved -maximal if burns cover 60% or more of the TBSA 1. Cardiovascular Response fluid loss > hypovolemia > decreased cardiac output > decreased BP > decreased perfusion and oxygen delivery

> onset of burn shock > sympathetic response > peripheral vasoconstriction > further decrease in the CO -the greatest volume of fluid leak occurs in 24 – 36 hours after the burn, peaking at 6 – 8 hours -basically caused by increased capillary permeability -diuresis occurs for several days to 2 weeks 2. Burn Edema -swelling maximal after 24 hours -begins to resolve 1-2 days post burn -completely resolved after 7-10 days post injury Edema > pressure on the small blood vessels and nerves of distal extremity > ischemia >

3. Effects on Fluids and Electrolytes and Blood Volume -evaporative loss through the burn wound (3-5 L) -hyponatremia (dilutional due to fluid shift from interstitial to intravascular space) -hyperkalemia due to massive cell destruction *later results in hypokalemia due to dilution caused by fluid shift -anemia due to blood loss and hemolysis (though may be seen as polycythemia due to excessive plasma loss) 4. Pulmonary Response -inhalation injury > release of histamine, serotonin and thromboxane > catecholamine release > hypoxia

-atelectasis may be present due to decreased surfactant -types of pulmonary injury: *upper airway injury -results from direct heat and edema *inhalation injury below the glottis -usually results from carbon monoxide poisoning -respiratory acidosis may occur over the first 5 days after the burn -indicators of a possible pulmonary damage; *hx indicating that burn occurred in an enclosed space *burns of the face and neck *singed nasal hair *hoarseness, voice change, dry cough, stridor *bloody sputum

*Labored breathing or tachypnea *Erythema or blistering of the oral or pharyngeal mucosa -possible consequences will be respiratory failure and acute respiratory distress syndrome 4. Other Systemic Responses -hemolysis and muscle damage > release of hemoglobin and myoglobin > acute tubular necrosis and renal failure -decreased immune response > sepsis -loss of skin tissue > altered thermoregulation > hypothermia > later hyperthermia due to hypermetabolism -sympathetic hyperactivity > paralytic ileus and Curling’s ulcer

Management: 1. Emergent/ Resuscitative Phase of Burn Care A. On the scene Care -airway, breathing and circulation -disability, exposure and fluid resuscitation -duration (from onset of injury to completion of fluid resuscitation -priorities: *first aid *prevention of shock *prevention of respiratory distress *detection and treatment of concomitant injuries *wound assessment and initial care

-emergency procedures at the burn scene: *extinguish the flames *cool the burn *remove restrictive objects *cover the wound *irrigate chemical burns B. Emergency Medical Management: -transport to the nearest hospital > life-saving measures -ABC -humidification, bronchodilation, mucolytic agents, coughing -ET tube insertion and assisted ventilation -continuous positive airway pressure -assessment for head and neck injuries

-burn wound management -IV access, CVP insertion -indwelling urinary catheter insertion -baseline data -tetanus prophylaxis -adequate pain relief C. Transfer to Burn Center D. Management of Fluid Loss and Shock -fluid replacement therapy -fluid requirements Problems Associated: >Acute Resp and Renal Failure >Distributive Shock > Compartment Syndrome

2. Acute or Intermediate Phase of Burn Care -begins 48 to 72 hours after the burn injury -goals: A. Infection Prevention -Staphylococcus, Pseudomonas, Proteus, E. coli, and Klebsiella -Candida is also being implicated -3 characteristics of burn wound sepsis: *100,000 bacteria/gram of tissue *inflammation *sludging and thrombosis of dermal blood vessels -early enteral feeding can be used for prevention

B. Wound Cleaning -hydrotherapy >use of tap water >temperature of water should be maintained at 37.8C >room temperature should be maintained at 26.6-29.4C >should be limited to a 20-30 minute period C. Topical Antibacterial therapy -criteria for choosing antibiotics: *effective against gram negative organisms *clinically effective

*penetrates the eschar but without systemic toxicity *does not lose its effectiveness *cost effective, available and acceptable *easy to apply -examples: 1. Silver sulfadiazine 2. Silver Nitrate 3. Mafenide Acetate D. Wound Dressing E. Dressing Changes F. Wound Debridement -2 goals: *to remove tissue contaminated by bacteria

*to remove devitalized tissue or burn eschar in preparation for grafting and wound healing G. Pain Management H. Nutritional Support

Shock -types: 1. Hypovolemic Shock 2. Cardiogenic Shock 3. Circulatory Shock (Distributive Shock) > Septic Shock > Neurogenic Shock > Anaphylactic Shock *Obstructive Shock -Effect of shock to normal cellular functions -Vascular Responses 1. Central Regulatory Mechanisms 2. Local Regulatory Mechanisms

-Blood Pressure Regulation BP= CO x TPR CO= SV x HR >Maintained by: a. nervous system b. endocrine system c. chemicals >Maintain tissue/organ perfusion: a. MAP= systolic BP + 2 (diastolic BP) 3 *should exceed 70-80 mmHg -Stages of Shock 1. Compensatory Stage >BP is maintained within normal limits due to the effect of normally functioning regulatory mechanisms

>s/sx: *metabolic acidosis *mental status change *tachypnea >medical management: a. identify the cause of shock b. correction of shock c. support of the regulatory mechanisms >nursing management: a. monitoring tissue perfusion *LOC *urine output *V/S *skin *laboratory values

b. reducing anxiety c. promoting safety 2. Progressive Stage -exhaustion of the compensatory mechanisms *myocardial depression *increased capillary permeability -assessment and dxtic findings: a. respiratory effects hypoxemia and hypercarbia intense inflammatory response decreased surfactant production acute respiratory distress syndrome (acute lung injury, shock lung, non cardiogenic pulmonary edema)

b. cardiovascular effects dysrhythmias myocardial infarction cardiac depression c. neurologic effects decreased cerebral perfusion *mental status change *behavioral change *pupillary dilation d. renal effects MAP<80mmHg acute renal failure

e. hepatic effects decreased blood flow less ability to perform hepatic functions f. gastrointestinal effects decreased blood flow *PUD *bloody diarrhea *sepsis g. hematologic DIC shock

-medical management: a. depends on the type of shock b. depends on the decompensation of the organ systems Management Common To All Types Of Shock a. optimize intravascular volume b. supporting the pumping action of the heart c. improving the competence of the vascular system Nursing Management: a. preventing complications b. promoting rest and comfort c. supporting family members

3. Irreversible Stage -severe organ damage -can no longer respond to treatment -survival is less likely -medical management: a. same with the progressive stage -nursing management: a. same with progressive shock b. moral support to the family c. ethical issues (living will)

Clinical Findings in the Stages of Shock Finding

Compensatory

Progressive

Irreversible

BP

normal

Systolic <80 -90mmHg

Mechanical or pharma support

HR

>100bpm

>150bpm

erratic, asystole

Respiration >20 breaths/ min

Rapid, shallow crackles

Intubation

Skin

cold, clammy

Mottled, petechiae

Jaundice

Urine Output

decreased

0.5ml/kg/hr

anuria, needs dialysis

Mentation

confusion

Lethargy

Coma

Finding

Compensatory

A/B Balance Resp Alkalosis

Progressive Met Acidosis

Irreversible Profound Acidosis

HYPOVOLEMIC SHOCK -most common type of shock -characterized by decreased intravascular volume of 15-25% -predisposing factors: External: Fluid Losses Internal: Fluid Shifts a. trauma a. hemorrhage b. surgery b. burns c. vomiting c. ascites d. diarrhea d. peritonitis e. diuresis e. dehydration f. diabetes insipidus

-medical management: >goals: a. restore intravascular volume b. redistribute fluid volume c. correct the underlying cause *pharmacologic therapy desmopressin anti-emetic insulin anti-diarrhea -nursing management: a. administering blood and fluids safely

CARDIOGENIC SHOCK -due to cardiac failure -either coronary and non coronary Coronary Factors Non Coronary Factors a. myocardial infarction a. cardiomyopathies b. valvular damage c. cardiac tamponade d. dysrhythmias -signs and symptoms: a. anginal pain b. hemodynamic instability c. dysrhythmias -medical management: a. correction of underlying cause

b. initiation of first line treatment *supplemental oxygen *vasoactive medications *controlling chest pain *controlling HR *selected fluid support *mechanical cardiac support c. pharmacologic therapy *dobutamine *nitroglycerine *dopamine *vasoactive meds *anti-arrhythmic meds d. fluid therapy -nursing management: a. preventing cardiogenic shock b. administering meds and IV fluids

c. maintaining mechanical devices d. enhancing safety and comfort CIRCULATORY SHOCK vasodilation maldistribution of blood volume decreased venous return decreased stroke volume decreased cardiac output decreased tissue perfusion A. Septic Shock -risk factors: a. immunosuppression

b. extremes of age d. chronic illness c. malnutrition e. invasive procedures -medical management: a. pharmacologic therapy b. nutritional therapy -nursing management: a. supportive to the medical management B. Neurogenic Shock -occurs due to the loss of sympathetic tone -predisposing factors: a. spinal cord injury c. depressant meds b. spinal anesthesia d. hypoglycemia

-medical management: a. restoring sympathetic tone -nursing management: a. elevate the head of the bed 30 degrees ( in spinal/epidural anesthesia) b. immobilize the patient (in spinal cord injury) c. elastic compression stockings d. feet elevation e. heparin/low molecular weight heparin f. pneumatic compression of the legs g. passive ROM

C. Anaphylactic Shock antigen-antibody reaction brought about by severe allergic reaction provokes mast cells to release chemical mediators like histamine and bradykinin widespread vasodilatation and capillary permeability -predisposing factors: a. drug sensitivity c. bee sting allergy b. transfusion reaction d. latex sensitivity -medical management: a. removal of the causative agent b. restore vascular tone (epinephrine) c. antihistamines and bronchodilators

-nursing management: a. assess for previous hypersensitivity reactions b. prevention of future exposure to antigens c. identification of new antigens d. patient education

RENAL DISEASES Terms: 1. aldosterone 2. antidiuretic hormone 3. anuria 4. bacteriuria 5. clearance 6. dysuria 7. frequency 8. GFR

9. hematuria 10. nocturia 11. oliguria 12. proteinuria 13. pyuria 14. Valsalva Leak Point Maneuver 15. vesicoureteral reflux

Test of Urine Specific Gravity: 1. Osmolality 2. Specific gravity

Kidneys -retroperitoneal organs -120 – 170g -12cm long, 6cm wide and 2.5cm thick -with 8 – 18 pyramids -with 4 -13 minor calyces -with 2 – 3 major calyces -with protective structures: a. Pararenal fat b. Gerota’s fascia c. Perirenal fat d. Renal capsule

Nephron -basic structural and functional unit of the kidney

3 Processes of Urine Formation 1. Glomerular Filtration 2. Tubular Reabsorption 3. Tubular Secretion  Renal function begins to decrease at a rate of 1% each year at 30. A. Acute Pyelonephritis -bacterial infection of the renal pelvis, tubules and interstitial tissue -an ascending infection -predisposing factors: a. vesico-ureteral reflux b. urinary tract obstruction 

-enlarged kidney -with abscess on the renal capsule and at the cortico-medullary junction -s/sx: >fever and chills >costo-vertebral angle >leucocytosis tenderness >bacteriuria and >flank pain pyuria dysuria >inc. urinary frequency -dx: >UTZ >Nuclear scan >CT scan >IVP >Urine Culture & Sensitivity Test

Medical Management: a. uncomplicated -no dehydration, no nausea and vomiting, no sepsis >2 weeks of oral antibiotics Trimethoprim-Sulfamethoxazole Ciprofloxacin Gentamicin with or without Ampicillin Third Generation Cephalosporins >6 weeks of oral antibiotics if with relapse *urine culture 2 weeks after antibiotic therapy b. complicated -pregnant patients >hospitalization (antibiotics from IV to oral)

B. Chronic Pyelonephritis -repeated acute pyelonephritis >> chronic pyelonephritis -no s/sx unless there’s an acute exacerbation -kidneys scarred, contracted and non functional -signs and symptoms: fatigue polyuria headache excessive thirst anorexia weight loss -diagnosis: creatinine and BUN clearance creatinine levels intravenous pyelography

-complications: a. ESRD b. hypertension c. formation of renal stones -may be due to the presence of urea splitting microorganisms -medical management: a. urine culture and sensitivity guided antibiotic therapy Nitrofurantoin TMP-SMZ -nursing management: a. monitoring -I&O b. oral fluids (3-4L/day)

c. symptomatic -antipyretics d. education -advise bed rest -prevention of UTI C. Acute Glomerulonephritis -primarily a disease of children older than 2 years old -may affect any age -causes: >autoimmune SLE >streptococcal Acute Post Streptococcal Glomerulonephritis

Acute Post Streptococcal Glomerulonephritis -2 to 3 weeks after >impetigo >sorethroat -signs and symptoms: hematuria tea colored urine proteinuria inc serum BUN and crea anemia edema

hypertension headache, malaise, flank pain (+) kidney punch congestion confusion, somnolence and seizures

Group A Beta-Hemolytic Streptococcal Infection Antigen-Antibody Reaction Deposition in the Glomerulus Increased Production of Epithelial Cells in the Glomerulus WBC Infiltration Thickening Scarring Decreased GFR -diagnosis: a. kidney biopsy b. electron microscopy c. immunoflourescence analysis

d. Anti-Streptolysin O Titer Anti-DNAse B Titer e. Serum Complement Determination -decreased -will normalize in 2 – 8 weeks IgA Nephropathy -most common type of primary glomerulonephritis -Inc IgA; with normal serum complement -complications: a. Hypertensive Encephalopathy b. Heart Failure c. Pulmonary Edema

Rapidly Progressive Glomerulonephritis -patient deteriorates in weeks to months -course is more severe and more rapid Management To Glomerulonephritis Goals: 1. Treat symptoms 2. Preserve renal function 3. Treat complications a. antibiotics b. steroids c. cytotoxic agents

d. protein restriction e. sodium restriction f. diuretics g. dialysis

D. Chronic Glomerulonephritis -components: repeated acute glomerulonephritis hypertensive nephrosclerosis hyperlipidemia chronic tubulo-interstitial injury hemodynamically mediated glomerular sclerosis -contraction of the kidneys to 1/5 of its original size -deformed kidneys -may result to ESRD -signs and symptoms: may be asymptomatic hypertension inc BUN and Crea bipedal edema

retinal hemorrhages ophthalmoscopy papilledema weight loss weakness and irritability nocturia GIT disturbances anemia heart failure peripheral neuropathy, decreased DTR pulsus paradosus -diagnosis: 1. Urinalysis - fixed sp. Gravity at 1.010 proteinuria; urinary casts

2. serum chemistry -hyperkalemia -hypoalbuminemia -hyperphosphatemia -hypocalcemia -hypermagnesemia 3. CBC -anemia 4. Chest X-Ray -cardiomegaly -pulmonary edema 5. ECG -left ventricular hypertrophy

-management: 1. treatment of hypertension 2. weight monitoring 3. give proteins of high biologic value 4. adequate calories 5. dialysis -nursing management: 1. monitoring E. Nephrotic Syndrome -components: proteinuria hyperlipidemia hypoalbuminemia

-causes: a. chronic glomerulonephritis b. diabetes mellitus c. amyloidosis d. SLE e. multiple myeloma f. renal vein thrombosis -signs and symptoms: edema (soft and pitting) -eyes, dependent area and abdomen malaise irritability headache fatigue

-diagnosis: 1. Urinalysis -proteinuria (3-3.5g/day) -inc WBC 2. Protein Electrophoresis Immunoelectrophoresis 3. Biopsy 4. AntiC1q antibodies (SLE) -complications: a. infection d. acute RF b. thromboembolism e. pulmonary emboli c. accelerated atherosclerosis

-management: 1. diuretics 2. ACE inhibitors 3. immunosuppressants 4. steroids 5. hypolipidemic agents 6. sodium restriction 7. CHON intake of 0.8g/kg/day low saturated fats



Urolithiasis -stones or calculi in the urinary tract -supersaturation of substances such as calcium oxalate, calcium phosphate and uric acid -signs and symptoms: >depends on: *the site of obstruction *edema *infection -assessment and diagnosis >IVP, Intravenous Urography >Retrograde Pyelography >UTZ >serum chemistries and 24 urine tests

deficiency of citrate, mg nephrocalcin & uropontin dehydration infection

Urolithiasis urinary stasis periods of immobility hypercalciuria and hypercalcemia

-causes of hypercalcemia and hypercalciuria: a. hyperparathyroidism b. renal tubular acidosis c. cancers d. granulomatous disease e. excessive intake of Vitamin D f. excessive intake of milk and alkali g. myeloproliferative disease -substances other than calcium that may precipitate and form stones a. uric acid -5%-10% of renal stones -gout, myeloproliferative disorders

b. struvite -15% of renal stones -in persistently alkaline and ammonia rich urine (caused by urease-splitting bacteria) -in neurogenic bladder, foreign bodies and recurrent UTI c. cystine -1%-2% of renal stones -hereditary defect in the renal absorption -medicines that increases the risk of urolithiasis a. acetazolamide d. laxatives b. Vitamin D e. high doses of aspirin c. antacids

-management: a. eradicate the stone b. determine the stone type c. prevent nephron destruction d. control infection e. relieve any obstruction >Opioid Analgesics NSAIDs >Hot Baths and Moist Heat to the flank area >Advise to increase oral fluid intake (urine output of >2L/day is advisable)

-specific management: 1. Calcium stones -restrict proteins and sodium in the diet -acidify the urine using Ammonium chloride or Acetohydroxamic Acid -Cellulose sodium phosphate (binds calcium from food) -thiazide diuretics (if caused by inc PTH) 2. Uric Acid Stones -low purine diet (shellfish, mushrooms, asparagus, organ meats) -Allopurinol -alkalinize the urine

3. Cystine -low protein diet -penicillamine (to decrease excretion through the urine) 4. Oxalate -dilute the urine -limit oxalate containing foods (spinach, strawberries, rhubarb, tea, peanuts and wheat bran) -surgical management: a. Ureteroscopy b. Extracorporeal Shock Wave Lithotripsy c. Percutaneous Nephrostomy or Nephrolithotomy



Acute Renal Failure

-sudden and almost complete loss of renal function -signs and symptoms: *oliguria *normal urine output *anuria *rising serum creatinine and BUN Categories of ARF 1. Prerenal -shock 2. Intrarenal -the result of actual parenchymal damage -use of nephrotoxic drugs (NSAIDs and ACE inh)

3. Postrenal -the result of an obstruction in the distal urinary tract Four Clinical Phases of ARF 1. Initiation -begins with the initial insult and ends when oliguria develops 2. Oliguria -rise in the serum of waste products of metabolism -rise in serum potassium and magnesium 3. Diuresis -with gradually increasing urine output -renal function may still be markedly abnormal

4. Recovery Period -improvement of renal function -may take 3-12 months -with normal laboratory values -with permanent 1-3% reduction in GFR

Characteristics

Prerenal

Intrarenal

Postrenal

Etiology

hypoperfusion parenchymal obstruction damage

BUN value

increased

increased

Increased

Creatinine value increased

increased

Increased

Urine output

decreased

varies, often decreased

Urine sodium

Decreased, <20mEq/L

Increased, >40mEq/L

varies, may be decreased or anuria Varies, often <20mEq/L

Urinary Sediment

Normal, few hyaline casts

Abnormal casts

Usually normal

Characteristics Prerenal Urine osmolality Increased to 500mOms Urine specific Increased gravity

Intrarenal Abnormal casts and debris Low normal, 1.010

Postrenal Usually normal Varies

-associated problems: *metabolic acidosis *hyperphophatemia and hypocalcemia *anemia -prevention: *prevention of exposure to nephrotoxic drugs -aminoglycosides, cyclosporine, amphotericinB *serum BUN and creatinine monitoring -management: a. restore chemical balance and prevent complications b. identification and treatment of the underlying cause c. maintain fluid balance -BP, CVP, serum and urine elect., fluid loses

d. monitoring for over hydration -dyspnea, crackles, distended neck veins -Furosemide, Ethacrynic Acid e. dialysis -to prevent serious complications *hyperkalemia *severe metabolic acidosis *pericarditis *pulmonary edema f. pharmacologic -cation exchange resin (sodium polystyrene sulfonate-kayexalate)

-retention enema -diuretic therapy -low dopamine dose (1-3g/kg) -phosphate binding agents (AlOH) g. nutritional therapy -give additional proteins (1g/kg/day during the oliguric phase) -high potassium and phosphate foods are restricted (banana, citrus and coffee) -potassium restricted to 20-40mEq/day -sodium restricted to 2g/day -may require parenteral nutrition

-nursing management: a. monitoring fluid and electrolyte balance b. reducing metabolic rate -bed rest, prevention of fever and infection c. promoting pulmonary function -assistance in changing positions -advise to cough and deep breath d. preventing infection -asepsis -avoid inserting an indwelling urinary catheter e. providing skin care f. providing support



Chronic Renal Failure -is a progressive irreversible deterioration in renal function -with uremia or azotemia (severity of build up will be proportional to the severity of s/sx) -prognosis will be determined by the presence or absence of hypertension and proteinuria -causes: *diabetes mellitus- most common *hypertension *chronic glomerulonephritis *obstruction of the urinary tract *polycystic kidney disease *infections

- stages: Stage 1 -Reduced Renal Reserve -40%-75% loss of nephron function -usually asymptomatic Stage 2 -Renal Insufficiency -75%-90% loss of nephron function -increase in serum BUN and creatinine -inability to concentrate urine -anemia may develop -with polyuria and nocturia

Stage 3 -End Stage Renal Disease -<10% of nephron function remaining -regulatory, excretory and hormonal functions are lost -requires dialysis -signs and symptoms: cardiovascular *hypertension *pulmonary edema *heart failure *pericarditis dermatologic *pruritus *uremic frost (deposit of urea crystals) GI and Neurologic s&sx

-assessment and diagnosis a. glomerular filtration rate creatinine clearance b. serum electrolytes c. ABG d. CBC -complications a. Hyperkalemia b. Pericarditis, Pleural Effusion and Cardiac Tamponade c. Hypertension d. Anemia e. Bone Disease

-medical management: a. maintain kidney function and homeostasis b. treat the underlying cause and contributory factors >medications >dialysis >diet therapy 1. Pharmacologic Therapy a. antihypertensives > includes intravascular volume control *fluid restriction *sodium restriction b. sodium bicarbonate c. erythropoietin >will achieve a Hct of 33%-38%

>IV or SC 3x a week >takes 2-6 weeks to increase Hct >A/R: *hypertension *increased clotting of vascular access sites *seizures *depletion of body iron stores d. iron supplementation e. antiseizure agents >Diazepam >Phenytoin f. antacids

>aluminum based antacids neurologic symptoms osteomalacia >calcium carbonate 2. Nutritional Therapy -regulation of protein intake -regulation of fluid intake (500-600ml more than the previous day’s 24 hour UO) -regulation of sodium intake -regulation of potassium -adequate calories and vitamins 3. Dialysis -to prevent hyperkalemia

-nursing management: a. avoid the complications of reduced renal function b. assess fluid status c. identify potential sources of the imbalance d. implement a dietary program e. encourage self care and independence

Cardiovascular System Definition of Terms 1. Preload – venous blood return; degree of stretch of cardiac muscle fibers at the end of diastole 2. Afterload – BP in artery; amt of resistance to ejection of blood from ventricle 3. Depolarization – active; caused by entry of Na while K exits cell 4. Repolarization – rest; caused by reentry of K to the cell while Na exits 5. Systole – blood supply to all except the heart; ventricular contraction from ejection of blood from ventricles to pulmonary artery and aorta

6. Diastole – blood supply to the heart; period of ventricular relaxation resulting in ventricular filling 7. Cardiac Output – blood volume per minute; normal = 5L/min (resting adult heart) 8. Stroke Volume – blood volume per contraction; normal = 70mL (resting heart) 9. Baroreceptors – nerve fibers located in the aortic arch and carotid arteries that are responsible for reflex control of BP 10. Postural/ Orthostatic Hypotension – result to syncope (blood drops to brain = faint); usually 10mmHg systolic or more



Anatomy and Physiology 1. Heart Valves 2. Heart Chambers 3. Coronary Arteries 4. Cardiac Muscle 5. Cardiac Conduction System 6. Cardiac Hemodynamics >Cardiac Pressures *right ventricular systole (15-25mmHg) *PA diastolic pressure (8-15mmHg)

*left ventricular systole (110-130mmHg) *resting aortic pressure (80mmHg)

*4-12mmHg on both ventricles and atria at the end of diastole 7. Cardiac Output preload afterload stroke volume contractility baroreceptors 

Gender Differences 1. resting rate 2. stroke volume 3. ejection fraction

heart rate

higher in women



4. conduction time is briefer in women 5. arteries occlude more easily in women with atherosclerosis 6. effects of estrogen in cardiovascular system of women -regulation of vasomotor tone -response to vascular injury -good liver function -increased coagulation proteins -decreased fibrinolytic substances Diagnostic Work-ups Purposes: 1. to aid in the diagnosis of diseases 2. for prognostication 3. to screen patients at risk of diseases

4. monitor serum concentration of meds 5. monitor therapeutic effects of meds A. Cardiac Enzymes >Creatine Kinase (CK) *MB -most specific enzyme for MI -first enzyme level to rise in MI *MM and BB -other isoenzymes >Lactate Dehydrogenase -peaks 2-3days after MI >Myoglobin -starts to increase 1-3hours after MI; 4-12hours (peak)

>Troponin I -contractile proteins found in cardiac muscles only -starts to rise 3-4 hours after MI -peaks in 4-24 hours and remain elevated for 1-3 weeks B. Blood Chemistry >Lipid Profile *Total Cholesterol -should be less than 200mg/dl *Serum Lipoproteins LDL - should be less than 130mg/dl HDL - should be 35-65mg/dl in men - should be less than 35 to 85mg/dl in F TAG - should be 40-150mg/dl

Factors that may elevate TAG level: 1. obesity 2. alcohol use 3. diabetes Factors that contribute variations in cholesterol level: 1. age 4. exercise 7. tobacco use 2. gender 5. genetics 8. stress level 3. diet 6. menopause Factors that lower HDL level 1. smoking 4. physical inactivity 2. diabetes 3. obesity

>Serum Electrolytes >BUN and Creatinine >Serum Glucose Level C. Coagulation Studies >PTT -effects of Heparin therapy -intrinsic pathway -1.5 to 2.5x of their baseline values >PT -effects of Warfarin therapy -extrinsic pathway -2.5-3.5x (INR)

D. Hematologic Studies >CBC -WBC monitoring in immunocompromised patient after heart transplantation -associated anemia will aggravate CAD E. Chest X-Ray -for the evaluation of the size, position and contour of the heart -cardiac and pericardial calcification F. ECG >Continuous ECG Monitoring a. Hardwire Cardiac Monitoring b. Telemetry c. Transtelephoning

G. Cardiac Stress Testing a. Exercise Stress Test -by using a treadmill or stationary bike b. Pharmacologic Stress Test -by using Dipyridamole or Adenosine c. Emotional Stress Test Purposes of Cardiac Stress Test >to evaluate CAD >to determine the cause of chest pain >to assess the functional capacity of the heart after MI or surgery >to evaluate the effectiveness of anti-anginal drugs >to evaluate dysrhythmias after physical exercise >to determine specific goals for a fitness program

H. Echocardiography -to determine: a. pericardial effusions b. etiology of heart murmurs c. function of prosthetic heart valves d. chamber size e. ventricular wall motion *Transesophageal Echocardiography -with 6 hours of fasting prior -IV line -with local anesthetic and sedation -BP and ECG monitoring

-after the study: extension of fasting for another 4 hours monitoring for 30 – 60 minutes sorethroat for the next 24 hours I. Radionuclide Imaging >to evaluate: a. coronary artery perfusion b. myocardial ischemia and infarction c. left ventricular function >uses: Thallium 201 emits gamma rays Technetium 99m detected by scintillation camera

>types: a. Myocardial Perfusion Imaging b. Computed Tomography c. Positron Emission Tomography d. Magnetic Resonance Imaging J. Cardiac Catheterization -catheter advancement guided by fluoroscopy -to measure oxygen saturation and pressures on right and left side of the heart -needs: a. IV line b. BP and ECG monitoring c. resuscitation equipment at bedside -uses contrast agent (iodine based)

-complications: (right sided cardiac catheterization) a. dysrhythmias d. cardiac perforation b. venous spasm e. cardiac arrest c. infection -complications: (left sided cardiac catheterization) a. dysrhythmias d. systemic embolization b. MI c. perforation -nursing interventions (pre-op) 1. fasting for 8 – 12 hours 2. explain that the procedure will take 2 hours or less 3. with mild to moderate sedation 4. explain the anticipated sensations (flushing,

5. ask the patient to breath deeply or hold the breath >to lower the diaphram for better visualization >ask the patient to cough (to disrupt a dysrhythmia and to clear the contrast agent from the arteries) -nursing interventions (post-op): 1. observe the site for bleeding and hematoma 2. assess peripheral pulses on the same ext q 15mins for 4 hours then q 1 – 2 hours 3. evaluate temperature and color of the affected extremity 4. ask the patient to report signs and symptoms of arterial insufficiency (pain, numbness and tingling)

5. monitor for dysrhythmias and vasovagal reaction *bradycardia >may be *hypotension precipitated by a *nausea distended bladder >prompt interventions: -raise the feet and legs -administer IVF and IV atropine 6. explain that the patient should be in supine position for 2 – 6 hours 7. analgesics 8. report chest pain, bleeding and sudden discomfort 9. increase fluid intake to flush out the dye 10. watch out for orthostatic hypotension

Hemodynamic Monitoring 1. Central Venous Pressure 2. Pulmonary Artery Pressure 3. Intra-arterial BP Monitoring Central Venous Pressure -pressure in the vena cava or right atrium is used to: a. assess right ventricular function b. venous blood return to the right side of the heart -nursing interventions: a. application of dry, sterile dressing -should be dry and occlusive b. chest x-ray to confirm placement c. daily inspection for signs of infection (complication) 

d. watch out for air embolism (complication) e. maintenance of the transducer in phlebotactic axis *normal range: 0 – 8 mmHg >>> Pressure Monitoring System 3 – 8 cmH2O >> Water Manometer System Pulmonary Artery Pressure Monitoring -assessment of left ventricular function -etiology of shock -response to vasoactive medications -can measure: 1. CVP or right atrial pressure 2. pulmonary artery systolic and diastolic pressure (25/9 mmHg)

3. Mean Pulmonary Artery Pressure (15mmHg) 4. Pulmonary Artery Wedge Pressure (4.5 to 13 mmHg) -nursing interventions: a. Maintenance of the transducer at phlebotactic axis b. Watch out for complications: -infections -pulmonary artery rupture -pulmonary thromboembolism -pulmonary infarction -catheter kinking -dysrhythmias -air embolism

Intra-arterial BP Monitoring -direct and continuous BP measurements -ABG measurements -to obtain blood samples *after selection of an area (site)>> assess collateral circulation a. Allen’s test b. Doppler test -nursing interventions: a. observe asepsis b. watch out for complications: -local obstruction with distal ischemia -external hemorrhage -massive ecchymosis

-dissection -air embolism -blood loss -pain -arteriospasm -infection 

Hypertension -terms related: >hypertensive emergency >hypertensive urgency >rebound hypertension -types: a. Primary Hypertension

b. Secondary Hypertension

-BP monitoring: *normal BP >> *high normal >> *first stage >> *second stage >> *third stage >> -as a sign -as a risk factor -as a disease -risk factors: a. smoking b. dyslipidemia c. diabetes mellitus

recheck in 2 years recheck in 1 year confirm in 2 months confirm in 1 month confirm immediately

d. age older than 60 years e. gender (men) f. family history of CVD

-hypothesis: a. increased sympathetic activity b. renin-angiotensin-aldosterone system c. increased absorption of chloride d. decreased vasodilation of arterioles -complications: a. myocardial infarction b. heart failure c. renal failure d. stroke/ cerebro-vascular accident e. impaired vision -gerontologic considerations: a. accumulation of atherosclerotic plaque

b. fragmentation of arterial elastins c. increased collagen deposits d. impaired vasodilatations -diagnosis: a. urinalysis f. creatinine clearance b. blood chemistry g. renin level c. 12-lead ECG h. 24 hour urine protein d. chest x-ray e. echocardiography -medical management: a. pharmacologic therapy b. dietary therapy

-nursing interventions: a. patient education >avoid risk factors >promote healthy lifestyle



Peripheral Arterial Occlusive Disease -usually involves the segment of the aorta below the renal artery to the popliteal artery -risk factors: a. age (elderly) b. diabetes mellitus -clinical manifestations: a. intermittent claudication b. coldness or numbness of the affected extremity c. skin and nail changes d. ulcerations and gangrene e. bruits f. diminished to absent peripheral pulses g. muscle atrophy

-medical management: a. pharmacologic therapy *Pentoxyphylline -increases RBC flexibility and decreases blood viscosity *Cilostazol -inhibits platelet aggregation -increases vasodilatation -inhibits smooth muscle proliferation *Aspirin, Ticlopidine, Clopidogrel -antiplatelets b. surgical management: vascular grafting endarterectomy

-nursing management: a. maintain circulation *doppler *pulses *color q 1 hour x 8 hours *temperature q 2 hours x *capillary refill 24 hours *motor and sensory b. monitoring for potential complications *urine output *CVP & PR *mental status *hematoma



c. avoidance of leg crossing or dependency of the lower extremity d. reduce edema -elevate the affected extremity -exercise e. stockings -may not be necessary Upper Extremity Arterial Occlussive Disease -due to: a. atherosclerosis b. trauma -clinical management: a. forearm claudication b. poor motor function

  

-diagnosis a. difference of 20mmHg of BP between 2 arms b. duplex ultrasonography c. transcranial doppler evaluation -management: a. surgery *PTA *carotid to subclavian artery bypass *axillary to axillary bypass *autogenous reimplantation of the subclavian to carotid artery Aneurism Aortic Dissection Raynaud’s Phenomenon



Deep Vein Thrombosis Venous thrombosis Thrombophlebitis/ Phlebothrombosis -of unknown cause -with predisposing factors: (Virchow’s triad) A. stasis of blood >heart failure >vasodilators >shock >immobility B. vessel wall injury >trauma >chemical irritation C. altered blood coagulation >abrupt withdrawal from anticoagulants

>OCP >severe blood dyscrasias -manifestations: a. nonspecific b. phlegmasia cerulea dolens >massive iliofemoral venous thrombosis >entire extremity is massively swollen, tense, painful and cool to touch *deep vein involvement -edema of the affected extremity -affected extremity is warmer to touch -tenderness

*superficial vein involvement -pain -redness -tenderness -warmth -assessment a. history >varicose veins >obese >hypercoagulation >elderly >neoplastic disease >OCP >cardiovascular disease >recent major surgery b. physical assessment -prevention a. application of elastic compression stockings

b. use of intermittent pneumatic compression device c. positioning d. exercise -medical management 1. anticoagulation therapy a. unfractionated heparin -sc or iv (intermittent infusion) for 57days -given with Warfarin -coagulation study monitoring b. low molecular weight heparin -with longer half life

-can be used in pregnant women -less toxic c. thrombolytic therapy -alteplase, reteplase, t-PA streptokinase -should be given within the first three -effects less significant after 5 days -surgical management >when pharmacologic therapy is contraindicated a. thrombectomy b. vena cava filter -nursing management a. assessing and monitoring anticoagulant therapy

b. monitoring and managing potential complications >bleeding >thrombocytopenia >drug interactions c. provide comfort >bed rest >elevation of the leg >elastic compression stockings >analgesics >application of warm moist packs d. intermittent pneumatic compression devises >with 35 to 55 mmHg

e. positioning >feet higher than the heart f. exercises >passive then active exercises >deep breathing exercises >early ambulation *avoid sitting for more than 2 hours *walking for at least 10minutes every after 2 hours



Varicose Veins -abnormally dilated, tortuous, superficial veins caused by the incompetent venous valves -may occur in the lower extremities and esophagus -predisposing factors >old age >pregnancy >prolonged standing >genetic predisposition -has 2 types: a. primary -without involvement of the deep veins

b. secondary -resulting from the obstruction of the deep veins -manifestations >dull aches >increased muscle >muscle cramps fatigue >ankle edema >feeling of heaviness -assessment a. duplex scan b. air plethysmography c. venography

-prevention a. avoidance of wearing tight socks or constricting panty girdle b. avoidance of crossing the thighs c. avoidance of prolonged standing d. frequent position changes e. elevating the affected extremity when tired f. walking 1 to 2 miles each day g. using the stairs instead of elevators h. elastic compression stockings i. weight reduction planning -management >surgery

>sclerotherapy -with application of elastic compression bandages for 5 days

Acquired Valvular Disorders 

Mitral Valve Prolapse -usually produces no symptoms -mostly in women -mitral valve balloons back into the left atrium during systole -signs and symptoms: -asymptomatic -palpitations -shortness of breath -syncope -light headedness -chest pain -dizziness -anxiety -diagnosis: -mitral clicks -murmur of mitral regurgitations

-medical management: a. symptomatic b. elimination of stimulants c. anti-arrhythmic meds d. beta blockers/ calcium channel blockers -nursing management: a. condition can be genetically transmitted b. use of prophylactic antibiotics -for patients with systolic click and a murmur c. instruct to avoid stimulants d. diet, activity and sleep



Mitral Regurgitation -signs and symptoms: a. chronic- asymptomatic b. acute - severe congestive heart failure dyspnea fatigue most common symptoms weakness palpitations shortness of breath on exertion cough -diagnosis: a. systolic murmur b. echocardiography



-medical management: similar to congestive heart failure Mitral Stenosis -causes rheumatic endocarditis -signs and symptoms: >dyspnea on exertion >fatigue (low cardiac output) >hemoptysis >cough -diagnosis: >weak pulses

>diastolic murmur -low pitched rumbling sound at the apex >echocardiography >ECG and cardiac catheterization with angiography -to determine the severity of mitral stenosis -medical management: a. prophylactic antibiotics b. anticoagulants c. treatment of CHF d. surgery -valvuloplasty -valve replacement



Aortic Regurgitation -causes: >endocarditis >syphilis >dissecting aneurism >deterioration of an aortic valve replacement -signs and symptoms: >asymptomatic >forceful heart beat (head and neck) exertional dyspnea and fatigue signs of left ventricular failure -diagnosis: >diastolic murmur (high pitched blowing sound)



>widened pulse pressure >water hammer pulse >echocardiography, ECG, MRI and cardiac catheterization -medical management: a. antibiotic prophylaxis b. valvuloplasty or valve replacement Aortic Stenosis -cause: *rheumatic endocarditis -signs and symptoms: >asymptomatic

>exertional dyspnea >dizziness

due to left ventricular failure

>syncope >chest pain -diagnosis: >systolic murmur -loud, rough -crescendo-decrescendo >12 lead ECG > echocardiography

-management: a. antibiotic prophylaxis b. valvuloplasty c. valve replacement

Cardiac Dysrhythmias  Sinus Node Dysrhythmias 1. Sinus Bradycardia -causes: *lower metabolic needs (hypothyroidism, hypothermia, sleep) *vagal stimulation (vomiting, suctioning, extreme pain) *medications (calcium channel blockers, beta blockers) *increased intracranial pressure *myocardial infarction -treatment: *atropine sulfate *catecholamines

2. Sinus Tachycardia -causes: *acute blood loss *pain *anemia *hypermetabolic state *shock *fever *hypervolemia *anxiety *hypovolemia *sympathomimetic meds *congestive heart failure -decreased diastolic filling decreased cardiac output -syncope -acute pulmonary edema -decreased BP

-management: a. Ca channel blockers b. Beta blockers 3. Sinus Arrhythmias -no significant hemodynamic effects -not treated usually  Atrial Dysrhythmias 1. Premature Atrial Complex -begins before the next impulse of the SA node -causes: >caffeine, alcohol nicotine >stretched atrial myocardium

>anxiety >hypokalemia >hypermetabolic state >atrial ischemia, injury or infarction -management: >directed toward the cause 2. Atrial Flutter -only at the atrium at a rate of 250-400/minute -therapeutic block at the AV node -causes: >advanced age >hypertension >valvular heart disease >cardiomyopathy >coronary artery disease >hyperthyroidism

>pulmonary disease >acute moderate to heavy ingestion of alcohol (holiday heart syndrome) >aftermath of open heart surgery -signs and symptoms: *chest pain *low BP *shortness of breath -management: >electrical cardioversion >if stable -digitalis -beta blockers -calcium channel blockers

3. Atrial Fibrillation -rapid, disorganized and uncoordinated twitching of atrial musculature -with decreased stroke volume -with decreased diastole >> decreased coronary artery perfusion >> increase the risk of myocardial ischemia -increased risk of thrombus formation within the atria >> embolism -2 to 5x increased risk of stroke -same causes as with atrial flutter -s/sx: *irregular palpitations *malaise

-treatment: >same as with atrial flutter >cardioversion (if present in less than 48 hours unless the patient is on anticoagulant treatment) >anti-arrhythmic meds: -amiodarone, flecainide, ibutilide >adenosine (treatment and diagnosis) >pacemaker insertion  Ventricular Dysrhythmias 1. Premature Ventricular Complex -an impulse that starts at the left ventricle and is conducted through the ventricles before the next normal sinus impulse -causes: *caffeine, nicotine and alcohol

*cardiac dysrhythmias and infarction *increased workload to the heart (exercise, fever, hypervolemia, heart failure, tachycardia) *digitalis toxicity *hypoxia, acidosis *electrolyte imbalances (hypokalemia) -with danger of ventricular tachycardia if with MI -bigeminy, trigeminy… -signs and symptoms: >asymptomatic >with skipped beats -treatment: >treat the cause Lidocaine- short term and immediate therapy

2. Ventricular Tachycardia -3 or more PVCs in a row occurring at a rate exceeding 100 beats/minute -causes are similar to PVCs -usually associated with CAD preceding to PVC -an emergency: pulseless and unresponsive -treatment: >if stable: -attach to ECG >if unstable: -cardioversion or defibrillation 3. Ventricular Fibrillation -rapid but disorganized ventricular rhythm -no atrial activity

-causes: >electrical shock >brugada syndrome -normal heart, few or no risk factor for CAD, and a family history of sudden cardiac death -signs and symptoms: >no heartbeat >no pulse >no respiration -management: >immediate defibrillation >vasoactive meds >anti-arrhythmic meds 4. Ventricular Asystole

HEMATOLOGY Hematologic System 1. Blood a. Plasma -albumin -globulin -fibrinogen -electrolytes -waste products b. cellular component -RBC -WBC -platelets

2. Reticulo-endothelial -liver -spleen -bone marrow







Functions of the blood a. carrier -oxygen and nutrients -waste products b. hemostasis Hematopoiesis a. intramedullary b. extramedullary RBC -approximately 8 micrometers -flexible, can pass through a small blood vessel -made up of hemoglobin (95% of cell mass)





Erythropoietin -response to low RBC count -stimulate the BM -for erythropoiesis >requires iron, folic acid, pyridoxine and cyanocobalamin Iron Stores and Metabolism -diet: >10-15 mg of elemental iron/day in a well balanced diet >only 0.5 to 1 mg is absorbed >> transferrin >> normoblast >> hemoglobin -total body iron content: >3 grams

-normal concentration value: >75-175ug/dl for males >65-165 ug/dl for females  Vitamin B12 and Folic Acid Metabolism -required in the synthesis of DNA ANEMIA 3 Broad Causes: 1. loss of RBC 2. inadequate production 3. increased destruction 1. Types of Anemia due to decreased production of RBC a. Iron Deficiency Anemia C. Folate Deficiency b. Vitamin B12 deficiency D. Dec. Erythropoietin

2. anemia due to blood loss 3. Types of anemia due to increased destruction (hemolytic) a. altered erythropoiesis >sickle cell anemia >thalassemia >hemoglobinopathies b. hypersplenism c. drug induced anemia d. autoimmune anemia  Clinical manifestations: (fatigue- most common) >severity depends on: 1. speed with which anemia has developed

2. duration of anemia 3. metabolic requirements of the individual 4. presence of other disorders  Complications: 1. Congestive Heart Failure 2. Paresthesia 3. Confusion  Nursing Diagnosis: 1. Activity Intolerance related to Fatigue, Weakness and Generalized Malaise 2. Altered Nutrition: Less than body Requirements related to Inadequate Intake of Essential Nutrients 3. Altered Tissue Perfusion r/t Inadequate Blood Volume

Nursing Interventions: 1. Managing fatigue -the most frequent symptom and complication -profound impact on ones level of functioning and quality of life 2. Maintain adequate nutrition -well balanced diet -avoidance of alcohol -dietary teaching -dietary supplements 3. Maintain adequate perfusion -transfusion -supplemental oxygen/vital signs monitoring 

4. Complying with prescribed therapy 5. Monitoring and managing potential complications a. CHF b. paresthesia c. confusion Hypoproliferative Anemias  Iron Deficiency Anemia -causes: >decreased dietary intake of iron >blood loss *menorrhagia *PUD (alcoholics)

-clinical manifestations: >smooth, sore tongue >brittle and ridged nails >angular cheilosis -diagnosis: a. BMA b. serum ferritin/TIBC c. peripheral blood smear (dec MCV) d. CBC (dec Hgb and Hct) -management: a. Iron supplementation (Ferrous SO4, Ferrous Fumarate or Ferrous Gluconate) -should be taken for 6-12 months

*if oral iron preparation is not tolerated, give iron dextran (IM or IV) -Nursing Management: 1. Diet -should take foods rich in iron *organ meats *green leafy vegetables *beans *raisins -should take foods rich in vitamin C -take iron with an empty stomach -if with GI distress, take with food (but absorption will be decreased by 50%) -liquid oral iron preparation



Anemia in Renal Disease -ESRD: >less likely to develop unless serum creatinine exceeds 3mg/dl -Dialysis: >may lose blood into the dializer >> folic acid deficiency and iron deficiency -Management: 1. Recombinant Erythropoietin >A/R: HPN- may inc Hct by 33-38% (dose needs to be titrated and administer antiHPN) 2. Oral iron and folic acid supplementation



Anemia of Chronic Diseases -due to chronic disease of inflammation, infection and/or malignancy -mild to moderate anemia -insidious onset over a period of 6-8 weeks -Hct seldom less than 25% -Hgb seldom less than 9 g/dl -erythropoietin levels are low -moderate shortening of the RBC lifespan -management: >no need >treatment of the underlying cause



Aplastic Anemia -may lead to pancytopenia -damage to the BM stem cells -replacement of the marrow with fat -also has neutropenia and thrombocytopenia -forms: >congenital >idiopathic >acquired -clinical manifestations: (insidious onset) >infection >anemia >bruising

-causes: 1. chemicals -pesticides -glue 2. medications -antimicrobials (Chloramphenicol) -gold compounds -sulfonamides -assessment and diagnosis: 1. BMA -medical management: 1. BM transplant or Peripheral Stem Cell Transplant 2. Immunosuppressive therapy

3. Withdrawal of the offending agent 4. RBC and platelet transfusion  Megaloblastic Anemia -may lead to pancytopenia -due to vitamin B12 and Folic Acid Deficiency (abnormal DNA synthesis) -Hgb may be as low as 4-5 gm/dl -WBC count may be as low as 2000-3000/mm3 -platelet count of less than 50000/mm3 -RBC (increase in MCV)  Folic Acid Deficiency -causes: *depletion in 4 months time without sufficient folic acid in the diet (green leafy vegetables and liver) *increased folic acid requirement (pregnancy,

alcoholism and chronic blood loss)  Cyanocobalamin deficiency -causes: *strict vegetarians (no meat or dairy products) *absence of intrinsic factor *faulty absorption in the ileum Clinical manifestations: a. Hemolytic s/sx -unique to vit B12 def b. GI and Nervous system effects Assessment and Diagnostic Findings: a. Schilling Test

-medical management: a. increase folic acid in the diet and take 1 mg of folic acid daily (IM for patients with malabsorption) b. Vit B12 replacement -oral supplements -fortified soy milk *if with intrinsic factor deficiency and malabsorption, monthly IM injection of cyanocobalamin at a dose of 1000ug -nursing management: a. mild jaundice b. vitiligo c. premature graying of the hair



d. smooth, red and sore tongue e. unstable gait f. impaired position and vibration sense Myelodysplastic Syndrome -is a group of disorder of myeloid stem cells causing dysplasia of one or more cell types -most common feature is the dysplasia of the RBCs >> macrocytic anemia (WBC & platelets may be affected) -may evolve into Acute Myeloid Leukemia -types: a. Primary >more than 80% (elderly) b. Secondary

-clinical manifestations: a. variable -assessment and diagnosis: a. CBC >RBC, WBC & platelets are decreased b. decreased serum erythropoietin -medical management: a. bone marrow transplantation b. blood transfusion (needs chelation of iron) c. platelet transfusion d. growth factors (G-CSF) e. erythropoietin

-nursing management: 1. prevention of infection 2. instructions on the risks of bleeding *chelation therapy is best administered as a subcutaneous infusion over 10-12 hours often at night *close monitoring of lab values for anticipation of transfusion and determination of response to growth factors

Hemolytic Anemias 

Sickle Cell Anemia -a result of inheritance of sickle hemoglobin gene -sickled Hgb *crystal formation when exposed to low oxygen tension, deformed, rigid and sickled RBC > ischemia & infarction

-sickling process is intermittent (with exposure to low oxygen tension and cold environment) -assessment and diagnostic findings >sickle cell trait: *normal RBC *normal WBC *normal platelets >sickle cell anemia *decreased Hct *sickled cells on smear -confirmatory test: Hemoglobin electrophoresis

-clinical manifestations: *Hgb 7-10mg/dl *jaundice *enlargement of the bones of the face and the skull *tachycardia, cardiac murmurs and enlarged heart *dysrhythmias and heart failure *susceptible to infection primarily pneumonia and osteomyelitis *chronic hemolysis and thrombosis >> ischemia and necrosis of organs with slowed circulation (spleen, lungs and CNS) -complications: 1. stroke

2. infection 3. renal failure 4. impotence 5. heart failure 6. pulmonary hypertension Sickle Cell Crisis -3 types: 1. Very painful sickle cell crisis > due to tissue hypoxia and necrosis 2. Aplastic crisis > due to infection of human parvovirus > Hgb decreases rapidly that the BM cannot compensate

3. Sequestration Crisis >pooling of sickled cells in an organ *spleen >> splenic infarction >> autosplenectomy Acute Chest Syndrome -decreased hemoglobin and hematocrit (rapid) -fever -tachycardia -bilateral chest film infiltrate -causes: -diagnostic tests: *infection *CXR *fat embolism *incentive spirometry -treatment: *bronchoscopy *antibiotics *phospholipase A2 det

*fluid restriction *corticosteroid *transfusion >decreases phospholipase A2 -prognosis: >usually diagnosed during childhood -medical management: >3 treatment modalities: a. BM transplantation b. Hydroxyurea *increases the concentration of fetal Hgb *decreases vaso-occlusive crisis c. Long term RBC transfusion

Adverse Effects of Hydroxyurea 1. chronic suppression of WBC formation 2. teratogenesis 3. potential for later development of pregnancy Complications of Transfusion 1. Iron Overload -needs chelation therapy 2. poor venous access 3. alloimmunization due to repeated transfusion *exchange transfusion Treatment: 1. Supportive >pain management

*folic acid supplementation 2. Prompt use of antibiotics -nursing diagnosis: 1. Pain related to tissue hypoxia 2. Risk for infection 3. Powerlessness related to illness induced powerlessness 4. Knowledge deficit regarding prevention of crisis -goals: 1. Relief of pain 2. Decreased incidence of crisis 3. Enhanced self esteem and power 4. Absence of complications

-nursing interventions: 1. Management of pain 2. preventing and managing infections 3. promoting coping skills 4. Minimizing knowledge deficit 5. Monitoring and managing potential complications -leg ulcers -priapism leading to impotence -chronic pain and substance abuse  Thalassemias -a hereditary disorder associated with defective hemoglobin chain synthesis -characterized by microcytosis and hypochromia

-imbalance in the configuration of hemoglobin >> increased rigidity of RBC >> hemolysis -2 types: (according to the globin chain diminished) a. alpha thalassemia -milder and often without symptoms b. beta thalassemia -more severe and lethal Alpha Thalassemia  Clinical Syndromes: 1. Silent Carrier -asymptomatic -deletion of a single alpha globin gene

-barely detectable reduction in alpha globin gene synthesis 2. Alpha Thalassemia Trait -deletion of 2 globin gene -minimal or no anemia and no abnormal physical signs 3. Hemoglobin H Disease -deletion of the 3 out of 4 alpha globin gene -hemoglobin H has extremely high O2 affinity and therefore not useful for O2 exchange -with moderately severe anemia 4. Hydrops fetalis -most severe form -deletion of the 4 alpha globin gene

-in the fetus > gamma globin chains in excess form tetramers (hemoglobin Bart) > extremely increased oxygen affinity > unable to deliver oxygen to the tissues > severe anoxia Beta Thalassemia  Clinical Syndromes: 1. Thalassemia Major -lead to severe transfusion dependent anemia -severe anemia and first become manifested 69mos after birth (hemoglobin synthesis switches from HgbF to HgbA) -if untransfused, Hgb may range between 36gm/dl (with marked anisocytosis and microcytic, hypochromic anemia)



-aggregated alpha chains are taken up by the spleen -increased reticulocytes but erythropoiesis is ineffective -clinical course: short or brief because of death at an early age 2. Thalassemia Minor -resistant against falcifarum malaria -asymptomatic and anemia is mild if present G6PD Deficiency (G6PD is essential for membrane stability) -would result to chronic hemolytic anemia -hemolysis only when under stress, infection or due to the use of certain medications (oxidant drugs) -inherited as X-linked disease

-oxidant drugs: >anti-malarial agents >sulfonamides >nitrofurantoin >analgesics (ASA, Phenacetin) >thiazides >chloramphenicol >para-amino-salisylic acid >vitamin K -clinical manifestations: >s/sx of hemolysis *reticulocytosis *jaundice *hemoglobinuria *pallor



-presence of Heinz bodies (taken up by the spleen) -assessment and diagnostic findings: >qualitative assay for G6PD -medical management: a. withdrawal of the offending agent b. transfusion -only in severe hemolytic states c. health education -avoid triggering factors Hereditary Spherocytosis -Is also a type of hemolytic anemia -Abnormal permeability of RBC membrane > spherocytosis > taken up by the liver > hemolysis



-treatment: >surgical removal of the spleen (splenectomy) Immune Hemolytic Anemia -due to exposure of RBCs to antibodies formation of alloantibodies destruction of RBCs (intravascular hemolysis) -usually result from hemolytic transfusion reactions -RBCs may be destroyed also because of poor level of suppressor lymphocytes > antibody formation (IgG) -2 types: 1. warm body antibodies >bind to RBCs most active in warm conditions

>most common (IgG usually but sometimes IgA) >mostly extravascular 2. Cold-body Antibodies >react in cold environment >usually IgM >usually occur acutely during recovery from viral infections, chronically with lymphoproliferative disorder >self limited intravascular hemolysis -clinical manifestations: (variable depending on the severity) a. splenomegaly in 80% of cases b. hepatomegaly c. lymphadenopathy d. jaundice

-assessment and diagnostic findings: a. CBC -decreased Hgb and Hct b. peripheral blood smear -increased reticulocytes c. serum chemistry -increased serum bilirubin -medical management: a. withdrawal of the offending agent b. increased doses of corticosteroids (1 mg/kg/day) c. blood transfusions -slowly and cautiously (10-15ml for 2030mins) d. splenectomy



e. immunosuppressive therapy -if splenectomy and steroids fail -cyclophosphamide (more rapid effect but more toxic) -azathioprine (less rapid effect but less toxic) f. Immunoglobulin administration -nursing management: a. prevention of infection *after splenectomy; during steroid and immunosuppressive therapy Hereditary Hemochromatosis -deposition of excessive iron in the liver, myocardium, testes, thyroid and pancreas

-women are less affected than men -signs and symptoms: a. weakness b. lethargy c. arthralgia d. weight loss e. loss of libido f. skin hyperpigmentation g. cardiac dysrrhythmias and cardiomyopathy > edema and dyspnea h. endocrine involvement *hypothyroidism *diminished libido *hypogonadism may lead to Hepatocellular Carcinoma

-diagnosis: a. liver biopsy -definitive test -medical management: a. therapeutic phlebotomy -removing whole blood from a vein -every 1–3 year period -nursing management: a. diet low in iron is not that important b. prevent liver injury such as alcoholism c. alpha feto-protein determination -serial screening test for hepatoma d. monitor for signs and symptoms of organ dysfunction

Polycythemia  Polycythemia Vera or Primary Polycythemia -may lead to Acute Myeloid Leukemia -myeloid stem cells have escaped normal control mechanisms -Increased RBC count (predominating sign) involvement of the spleen in hematopoiesis fibrosis of the bone marrow (burnt or spent phase) -signs and symptoms: >ruddy complexion >splenomegaly >pruritus (due to histamine)

>headache >dizziness >tinnitus >paresthesias >fatigue

due to an increased blood volume

>blurred vision >angina >claudication due to increased blood >dyspnea viscosity >thrombophlebitis >erythromyalgia - burning sensation of the fingers and toes

-assessment and diagnostic findings: 1. increased RBC mass (nuclear medicine procedure) -normal in erythropoietin 2. normal oxygen saturation level 3. enlarged spleen -other signs: 1. increased WBC and Platelet count 2. increased vitamin B12 3. increased alkaline phosphatase -complication 1. thrombosis - may lead to stroke or MI 2. bleeding

-medical management: 1. therapeutic phlebotomy >500ml once or twice weekly >to reduce the blood cell mass 2. radioactive phosphorus >to suppress marrow function but may increase the risk of leukemia -nursing management: 1. patient education >avoid Aspirin to decrease the risk >minimize alcohol of bleeding >cool or tepid water bath -for itchiness -antihistamines are not effective

Secondary Polycythemia -due to excessive production of erythropoietin as a reaction to: >smoking >COPD >cyanotic heart disease >increased altitude -medical management: 1. Therapeutic Phlebotomy Leukopenia and Neutropenia -may result from: *ionizing radiation *long term use of steroids 

*uremia *neoplasms -diagnosis: Absolute Neutrophil Count = % neutrophils + % bands X total WBC count 100 -clinical manifestations: infections -medical management: 1. withdrawal of the offending agent 2. corticosteroids 3. withholding or decreasing the dose of chemotherapy or radiotherapy 4. culture of blood, urine and sputum; CXR > monitoring

-nursing management: 1. infection control Bleeding Disorder -vascular in origin >> localized -platelets or coagulation factor defects >> widespread  Primary Thrombocythemia -also called essential thrombocythemia -stem cell disorder in the bone marrow -platelet count >> 600,000/mm3 >> size is abnormal increased RBC increased WBC

-clinical manifestations: >usually asymptomatic >hemorrhage or vasooclusion of the microvasculature >painful, burning, warmth and redness on the localized area of the extremity (due to an increased platelet ct.) -diagnosis: >CBC and other blood tests (not necessary to perform BMA and biopsy) *median survival is 10 years -medical management: (controversial) 1. Low Dose Aspirin -in young patient without aggravating factors like atherosclerosis, smoking and peripheral vascular disease

2. Hydroxyurea -chemotherapeutic agents to lower down the platelet count Anagrelide -more specific than Hydroxyurea -side effects: severe headache Alpha Interferon -lower the platelet count by unknown mechanisms -sc 3x a week -very expensive -side effects: >fatigue >dizziness >weakness >anemia >memory defects >liver dysfunction

3. Platelet Pheresis -to reduce platelets with transient effects -nursing management: 1. Patient education >risk of bleeding and thrombosis >signs of bleeding and thrombosis (visual changes, tingling and weakness)  Secondary Thrombocytosis -increased platelet production -an increase above 1 “M” count is rare -platelet function is normal >survival time is normal or increased



-triggering factors: >chronic inflammatory disorders >iron deficiency >acute hemorrhage >malignant disease >splenectomy Idiopathic Thrombocytopenic Purpura -affects all ages -more common to children and women -2 types: a. acute >predominantly in children >often 1-6 weeks after a viral illness >self-limited (remission within 6 months)

b. chronic -hypothetical causes: a. exposure to sulfa drugs, quinine b. SLE c. pregnancy d. autoimmunity -signs and symptoms: a. platelets >less than 20,000/mm3 or even less than 5,000/mm3 b. bruising, heavy menses and petechiae on the extremities and trunk

*2 types of purpura a. dry purpura -simple bruising or petechiae -tend to have fewer complications b. wet purpura -GIT bleeding -hemoptysis -intracranial bleeding -assessment and diagnostic findings: decreased platelet count decreased megakaryocytes

-management: a. safe platelet count -risk of bleeding starts at a platelet count of 10,000/mm3 and below b. withdrawal of the offending agent c. immunosuppressive therapy to inc -mainstay of short term treatment plt ct -to block the binding receptors in macrophages *Prednisone 1mg/kg -effective in 75% of cases -can be used also for maintenance at a dose of 2.5 to 10mg QOD *Cyclophosphamide

*Azathioprine *Dexamethasone *Vincristine d. intravenous immunoglobulin -binding the receptors on the macrophages -1g/kg for 2 days (very expensive) e. splenectomy -effective in 50% of cases -at risk of sepsis (should receive vaccines) *Pneumovax should be given *Haemophilus influenzae B within 2-3 wks *Meningococcal vaccines prior to proc

-nursing management: a. history taking -viral infection -intake of sulfa containing drugs b. neurologic assessment -in addition to physical examination -vital signs: don’t use the rectal route c. patient education -s/sx of bleeding -whom to contact in case of emergency -avoidance of sulfa containing drugs -compliance to pharmacologic therapy (tapering) -frequency of monitoring the platelet count

d. avoid the risk of bleeding -no constipation -use electric razors only -use soft bristled tooth brush -refrain from vigorous sexual intercourse e. education of the disadvantages of corticosteroid treatment -osteoporosis should receive Ca -proximal muscle wasting and vit D -dental caries supplements -cataract formation

Pulmonary Disorders 

Acute Respiratory Distress Syndrome -characteristics: (in the absence of LV Failure) *sudden or progressive pulmonary edema *increasing bilateral infiltrates on CXR *hypoxemia refractory to oxygen supplementation *reduced lung compliance -with a high mortality rate as high as 50-60% -multiple organ system failure with sepsis (most common cause of death)

acute lung injury alveolar capillary leak microvascular obstruction

a. pulmonary edema surfactant b. hyaline membrane defect c. microatelectasis decreased V/Q mismatch compliance right to left shunt pulmonary hypertension dyspnea hypoxemia increased dead space increased work of increased minute ventilation breathing

-causes: *aspiration (gastric acid) *drug ingestion and overdose *hematologic disorders -DIC, massive transfusion *prolonged inhalation of high concentrations of O2, smoke or corrosive substance *localized infection *metabolic disorders (pancreatitis) *shock *major surgery *fat or air embolism *sepsis

-signs and symptoms: *rapid onset of dyspnea -12 to 48 hours after the initiating event *arterial hypoxemia not responsive to O2 therapy *pulmonary edema -quickly worsen -assessment and diagnostics: *history and physical exam -retractions and crackles *CXR *pulse oximetry *ABG

-management: a. identification and treatment of the underlying condition b. aggressive, supportive care -intubation and mechanical ventilation c. circulatory support -IVF d. nutritional support (35-45kcal/kg/day) e. O2 inhalation f. PEEP (positive end expiratory pressure) -critical in ARDS -improves the oxygenation -increase the functional residual capacity

h. pharmacologic therapy -interleukin-1 receptor antagonist (anakinra) -neutrophil inhibitors -pulmonary specific vasodilators -surfactant replacement therapy -antisepsis therapy -antioxidant therapy -corticosteroids -nursing management: a. close monitoring b. respiratory modalities -O2 inhalation, nebulizer therapy, chest physiotherapy, ET intubation, suctioning, mechanical ventilation and bronchoscopy

c. positioning -to improve ventilation d. reduce anxiety and agitation -explain all procedure and provide care in a calm and reassuring manner e. continuous assessment (ventilator setting) -presence of tube blockade by kinking or retained secretions -acute respiratory problems (pneumothorax) -sudden hypoxemia -ventilator malfunction f. sedation -to decrease the patient’s O2 consumption

-to allow the ventilator provide full respiratory support -to decrease anxiety g. administration of neuromuscular blocking agents -alternative to sedation 

Acute Respiratory Failure -is a sudden life threatening deterioration of the gas exchange function of the lung -fall in arterial oxygen tension to less than 50mmHg and a rise in CO2 tension to more than 50mmHg and with an arterial pH of less than 7.35 -mechanisms: *alveolar hypoventilation *V/Q mismatch *diffusion abnormalities *shunting

-causes: a. decreased respiratory drive -severe brain injury -brainstem lesions -use of sedatives -metabolic disorders (hypothyroidism) b. dysfunction of the chest wall -diseases of the muscles, nerves, spinal cord and neuromuscular junction c. dysfunction of the lung parenchyma -pleural effusion -upper airway obstruction -pneumothorax

-signs and symptoms: *all related to hypoxemia and hypoxia restlessness dyspnea fatigue air hunger headache tachycardia and inc BP confusion, lethargy, tachycardia, tachypnea, central cyanosis respiratory arrest -management: a. correct the underlying cause b. restore adequate gas exchange (ET with ventilator)

surfactant replacement therapy antiseptic agents antioxidant therapy corticosteroids c. nutritional therapy  Chronic Obstructive Pulmonary Disease -airflow limitation not fully reversible -types: a. chronic bronchitis b. emphysema A. Chronic Bronchitis -cough with sputum for at least 3 months in each of 2 consecutive years

Smoke/environmental pollutants Hypersecretion of mucus and inflammation B. Emphysema Destruction of the walls of distended alveoli Impaired gas exchange -2 types: 1. panlobular >respiratory bronchiole, alveolar duct and alveoli are destroyed 2. centrilobular >destruction of the center of the secondary lobule -risk factors: 1. environmental >cigarette smoking

>prolonged and intense exposure to occupational dusts and chemicals >indoor air pollution >outdoor air pollution 2. host >alpha-1-antitrypsin deficiency -3 primary symptoms: a. cough b. sputum c. dyspnea on exertion -assessment and diagnosis: >spirometry -complications: a. respiratory failure

b. respiratory insufficiency -medical management: a. risk reduction b. pharmacologic therapy *bronchodilators >MDI >nebulization >oral (pill or liquid) beta adrenergic agonist anticholinergic agents methylxanthines *corticosteroids oral or IV (Beclomethasone, Fluticasone)

*vaccines >influenzae and pneumococcal *alpha-1-antitrypsin augmentation therapy *antibiotics *mucolytics *antitussives c. surgical management: *bullectomy *lung volume reduction surgery *lung transplantation -nursing management: a. patient education *breathing exercises

*inspiratory muscle training *activity pairing *self care activities *physical conditioning *oxygen therapy *nutritional therapy *coping measures



Asthma -a reversible chronic inflammatory disease of the airways -triad: *airway hyperresponsiveness *mucosal edema *excessive mucus production -signs and symptoms: *cough *wheezing *chest tightness *dyspnea -causes: a. allergy- strongest predisposing factor >seasonal (weed pollens, grass >perennial (molds, dust, roaches)

b. airway irritants (perfumes, smoke, cold, heat) c. exercise d. stress or emotional upset e. sinusitis f. medications g. viral respiratory tract infections h. gastro-esophageal reflux -pathophysiology bronchospasm mucosal edema exc mucus secretion bronchial muscle mucosal gland enlargement hypertrophy thick tenacious secretions alveolar hyperinflation

chronic asthma (chronic airway inflammation) airway subbasement membrane fibrosis airway narrowing irreversible airflow limitation

-signs and symptoms: *cough usually at night or early in the *dyspnea morning due to circadian *wheezing variations *diaphoresis *hypoxemia *tachycardia *central cyanosis *widened pulse pressure

-types according to severity: A. Mild Intermittent -symptoms <2 times a week -asymptomatic and normal PEF between exacerbations -exacerbations are brief; intensity may vary -night time symptoms <2 times a month B. Mild persistent -symptoms >2 times a week but <1 time a day -exacerbations may affect activity -night time symptoms >2 times a month C. Moderate Persistent -daily symptoms -daily use of inhaled short acting beta2 agonist

-exacerbations affect activity -exacerbations >2 times a week; may last days -night time symptoms >1 time a week D. Severe Persistent -continual symptoms -limited physical activity -frequent exacerbations -frequent night time symptoms

-assessment and diagnostics: *clinical history and physical assessment *sputum/blood tests >eosinophilia *serology >elevated IgE *ABG >hypoxemia >hypocapnia then hypercapnia *pulse oximetry >hypoxemia -prevention: a. identificaton and avoidance of allergens

-complications: a. status asthmaticus b. respiratory failure c. pneumonia d. atelectasis -medical management: a. Long Acting Medications *corticosteroids -most potent and effective -inhaled preparations commonly causes oral thrush -fluticasone, beclomethasone, budesonide

*mast cell stabilizer -for mild to moderate asthma only (prophylaxis) - cromolyn sodium and nedocromil *beta 2 agonist -to control symptoms especially at night -prophylaxis of exercise induced asthma -salmeterol, albuterol, formoterol *methylxanthines -mild to moderate bronchodilator -mainly for the relief of night time sx (theophylline as mild anti-inflammatory)

*leukotriene modifiers (inhibitors) -may be added or be used as an alternative to inhaled corticosteroids -zafirlukast, montelukast, zileuton B. Quick Relief Medications *short acting beta 2 agonist -to relieve acute symptoms -to prevent exercise induced asthma -may be combined with an anticholinergic -salbutamol, combivent (salbutamol+ipratropium bromide) >management of asthma exacerbation -early treatment and education of the patient



*quick relief medications *corticosteroids *O2 inhalation *serial measurement of lung function -peak flow meter (FEV) Status Asthmaticus -severe and persistent asthma that does not respond to conventional therapy -may last longer than 24 hours -causes: *infection *dehydration *anxiety *inc adrenergic blockage *nebulizer abuse *irritants (aspirin)

-pathophysiology: similar to bronchial asthma *hypoxemia and respiratory alkalosis >>> respiratory acidosis -signs and symptoms: similar to asthma (extent of wheezing does not indicate the severity of attack) -assessment and diagnosis: *pulmonary function study -most accurate *ABG -respiratory alkalosis (most frequent finding)



-medical management: *short acting beta adrenergic agonist and steroid *O2 inhalation *IVF *mechanical ventilation Bronchiectasis -is a chronic irreversible dilation of the bronchi and bronchioles -causes: *airway obstruction *diffuse airway injury *pulmonary infections and complications

*genetic disorders (cystic fibrosis) *abnormal host defense (ciliary dyskinesia) *idiopathic causes -pathophysiology: chronic airway inflammation bronchial wall damage bronchial obstruction (due to thick sputum) bronchial distention and distortion (localized; segmental/lobar-lower lobes usually) inflammation of the peribronchial tissues alveolar collapse pulmonary scarring/fibrosis

-signs and symptoms: *chronic cough *excessive production of purulent sputum *hemoptysis *clubbing of the fingers *repeated pulmonary infections -assessment and diagnosis: *history and physical assessment -prolonged history of productive cough *sputum exam -consistently negative for tubercle bacilli *CT scan -bronchial dilatation

-medical management: a. bronchial drainage -to clear excessive secretions -to prevent or control infection *postural drainage *bronchodilators *bronchoscopy *chest physiotherapy b. smoking cessation c. infection control -antimicrobial therapy (year round) -vaccination (influenza and pneumococcal pneumonia)

d. surgery -for patients who continue to expectorate large volume of phlegm -for patients with repeated bouts of pneumonia and hemoptysis *segmental resection *lobectomy *pneumonectomy -complications: *atelectasis *bronchopleural fistula *pneumonia *empyema

-nursing management: a. supportive and symptomatic b. assistance to clear secretions c. patient education -smoking cessation -infection prevention -postural drainage -activity/rest -nutrition

Pulmonary Edema -abnormal accumulation of fluids in the lung tissue and/or alveolar space -a severe, life threatening condition -causes: *left ventricular failure *hypervolemia *sudden increase in the intravascular pressure in the lungs (post operative pneumonectomy) >flash pulmonary edema

*rapid re-inflation of the lungs after the removal of air from a pneumothorax or evacuation of fluid from a large pleural effusion >re-expansion pulmonary edema -signs and symptoms: >increasing respiratory distress -dyspnea -central cyanosis -hunger -confusion/stupor >foamy, frothy, and often blood tinged secretions

-assessment and diagnostic findings: a. physical examination >crackles -initially in the base and posterior part of the lungs -progress toward the apices >tachycardia b. chest x-ray >increased interstitial markings c. pulse oximetry d. arterial blood gas determination -medical management: a. correction of the underlying cause b. vasodilators



c. inotropic agents d. afterload or preload agents e. contractility meds f. diuretics and fluid restriction g. oxygenation and mechanical ventilation h. morphine -nursing management: supportive to the medical management Pulmonary Hypertension -systolic pulmonary artery pressure exceeding 30mmHg -mean pulmonary artery pressure exceeding 25mmHg -2 Types: 1. Primary Pulmonary Hypertension

-with no evidence of pulmonary or cardiac disease or pulmonary embolism -more common in women 20-40 y/o -high mortality within 5 years of diagnosis 2. Secondary Pulmonary Hypertension -more common -secondary to existing cardiac and pulmonary disease (hypoxemia) -

Hypoxemia Hypercapnia Pulmonary Embolism Pulmonary Artery Constriction Increased Pulmonary Vascular resistance Increased Right Ventricular Workload Right Ventricular Hypertrophy Right Ventricular Failure

-signs and symptoms: *dyspnea -main symptom initially with exertion then eventually at rest *substernal chest pain *weakness *syncope *fatigue *occasional hemoptysis

*right sided heart failure -peripheral edema, ascites, neck vein engorgement, liver engorgement, crackles -assessment and diagnosis: *clinical history and physical examination *CXR *pulmonary function studies -normal, or slight decrease in VC and compliance -mild decrease in diffusing capacity *electrocardiogram -right ventricular hypertrophy -right axis deviation -tall peaked T waves (inferior leads) -tall R waves, ST segment depression, T wave inversion (anterior leads)

*echocardiogram -can assess the progression of the disease *ventilation perfusion scan -defects in the pulmonary vasculature such as pulmonary emboli *cardiac catheterization -elevated pulmonary arterial pressure *lung biopsy -through thoracotomy or thoracoscopy -medical management: Goal: 1. to manage the underlying cardiac or pulmonary condition

A. Supplemental Oxygen -reverses vasoconstriction -reduces pulmonary hypertension B. Pulmonary Vasodilators (calcium channel blockers, IV prostacyclin) -reduces pulmonary vascular resistance -increases the cardiac output C. Anticoagulants if with cor D. Fluid Restriction pulmonale E. Diuretics F. Cardiac Glycosides G. Heart-Lung Transplantation



-nursing management: 1. identify high risk patients -COPD, pulmonary emboli, congenital heart disease, mitral valve disease 2. monitor s/sx 3. administer oxygen therapy appropriately 4. home use oxygen supplementation Cor pulmonale -characterized by: a. right ventricular enlargement b. pulmonary congestion -causes: a. COPD -most frequent

b. deformities of the thoracic cage c. massive obesity d. primary embolism e. disorders of the nervous system f. disorders of the respiratory muscles g. disorders of the chest wall h. disorders of the pulmonary arterial tree Lung Disease Hypoxemia and Hypercapnia Pulmonary Hypertension Increased Work Load to the Right Ventricles Right Sided Heart Enlargement Right Sided Heart Failure

-signs and symptoms: *s/sx of the underlying pulmonary disease *s/sx of right sided heart failure -management: goals: 1. improvement of ventilation 2. treatment of the underlying lung disease 3. treatment of the manifestations of the heart A. Continuous 24 Hour O2 Therapy -improvement may require 4-6weeks of O2 therapy -monitor pulse oximetry and ABG

B. Chest Physiotherapy and Bronchial Hygiene Maneuvers C. Bronchodilators D. ET Intubation and Mechanical Ventilation E. Bed Rest F. Sodium Restriction G. Diuretic Therapy H. Digitalis Therapy I. ECG Monitoring -nursing management: *supportive to the medical management



Pulmonary Embolism -obstruction of the pulmonary artery or one of its branches by a thrombus or thrombi -causes: *venous thrombosis *atrial fibrillation Occlusion of the Pulmonary Artery Increased Alveolar Dead Space Ventilation/Perfusion Imbalance Hypoxemia and Hypercapnia Pulmonary Hypertension Right Ventricular Failure Shock

-signs and symptoms: *dyspnea -most frequent symptom *tachypnea -most frequent sign *chest pain -sudden and pleuritic -mimics angina pectoris *anxiety, fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, syncope -less than 10% progresses to pulmonary infarction -assessment and diagnosis: a. Ventilation Perfusion Scan (test of choice) b. Pulmonary Angiography (gold standard)

c. CXR -infiltrates -atelectasis -pleural effusion -elevation of the diaphragm d. ECG -sinus tachycardia -PR interval progression -non specific T wave changes e. Peripheral Vascular Studies f. ABG -prevention: *prevention of DEEP VEIN THROMBOSIS

-management: a. Emergency Management *Nasal O2 Therapy *IV access *Perfusion Scan, ABG, Hemodynamic Measurements *Dobutamine or Dopamine *ECG *Digitalis Glycosides, IV Diuretics and Antiarrhythmics when appropriate *Blood Studies *ET Intubation and Mechanical Ventilation *Indwelling Urinary Catheter Insertion *Small Doses of Sedatives or Morphine

b. General Management *O2 therapy *elastic compression stockings *intermittent pneumatic leg compression *elevation of the leg c. Pharmacologic Management *Anticoagulation Therapy Heparin (IV bolus of 5T to 10T “U” then infusion of 18U/kg/hour not to exceed 600U/hour) Warfarin (begun within 24 hours after initiating Heparin therapy) *Thrombolytic Therapy Urokinase, Streptokinase, Alteplase

CI:

CVA w/in the past 2 months active bleeding w/in the past 10 days recent labor & delivery severe hypertension d. Surgical Management: *embolectomy *interruption of the inferior vena cava Teflon clips -nursing management: a. Minimizing the risk of pulmonary embolism b. Preventing thrombus formation c. Assessing for potential pulmonary embolism d. Monitoring thrombolytic therapy

e. managing pain f. managing O2 therapy g. relieving anxiety h. monitoring for complications i. post op nursing care



Diabetic Ketoacidosis -is caused by an absent or markedly inadequate amount of insulin -results in disorder in the metabolism of carbohydrate, protein and fat -3 main clinical features of DKA: *hyperglycemia *dehydration and electrolyte loss *acidosis -assessment and diagnostic findings: *blood glucose level -300 to 800 mg/dl *serum bicarbonate -0-15mEq/L

*serum pH -low: 6.8-7.3 *PCO2 -low: 10-30mmHg -reflects respiratory compensation for acidosis *ketone bodies -elevated in the blood and in the urine *electrolyte depletion *BUN, creatinine, hgb and hct -elevated due to water loss

-lack of insulin increased breakdown of fat increased fatty acids increased ketone bodies -acetone breath -poor appetite -nausea

-decreased utilization of glucose by muscle, fat and liver -increased production of glucose by liver hyperglycemia

-blurred vision acidosis -nausea -vomiting -abdominal pain increasingly rapid respirations

polyuria dehydration -weakness -headache increased thirst

-prevention: a. full compliance to the medical treatment of diabetes mellitus b. good hydration c. good nutrition d. monitoring of blood and urine ketones every 3-4 hours -management: a. rehydration >6-10 L of IVF >plain NSS or half strength saline b. restoring electrolytes >ECG monitoring

*reversing acidosis: -insulin -nursing management: *same as in DM

Addison’s Disease

Cushing’s Syndrome

Sugar

Hypoglycemia, hyperkalemia

Hyperglycemia,hypokalemia

Salt

Hyponatremia

Hypernatremia

Sex

Decreased libido

Sexual urge not merely affected

Physical Appearance

Not seen, more on symptoms

Buffalo hump, moonface, pitting edema, hirsutism, breast atrophy, purple striae on abdomen, easy bruising, facial flushing, acne, hyperpigmentation

Diet

High Na, CHON, Low Na, CHO, fats but high CHO intake except K CHON and K intake

Hyperthyroidism (Thyroid Crisis)

Hypothyroidism (Myxedema Coma)

Grave’s Disease; inc. amt. of T3&T4

Dec. T3T4; causes in adult – myxedema, child cretinism

Inc. appetite – wt. loss due to inc. metabolism, heat intolerance, all VS increase, exopthalmos-pathognomonic symptom, amenorrhea

Dec. appetite – wt. gain due to decreased. metabolism, all VS decrease, decreased menstruation

Inc. caloric diet; watch out for thyrotoxicosis (triad): b. Tachycardia c. Hyperthermia d. agitation

Dec. caloric diet, force fluid

Meds: SSKI (Lugol’s solution), PTU prophylthiuracil

Meds: Levothyroxin (T4) synthroid

DKA Acute complication of type1 DM due to severe hyperglycemia, leading to CNS depression & coma

HHNS Hyperglycemia w/o ketosis is commonly on DM type2

Polyuria, Polydipsia, Hypotension, extreme thirst, Polyphagia, Glycosuria, dehydration, tachycardia, Pathognomonic hypokalemia, hyponatremia Sx: >acetone breath– fruity odor >kussmul’s respiration– rapid, shallow breathing Mx: monitor VS; I/O Meds: Insulin therapy (IV), counteract acidosis – Na HCO3

Tx: give insulin, inc. fluid